ライフサイエンスコーパス: plasma creatinine

1 eatinine clearance <60 ml/min or doubling of plasma creatinine).

2 hil and macrophage infiltration, and rise in plasma creatinine.

3 arance with elevated blood urea nitrogen and plasma creatinine.

4 tion along with decreased levels of ngal and plasma creatinine.

5 f allografts are still functioning with mean plasma creatinine 1.5 mg/dL.

6 e HO inhibitor had no effect on the level of plasma creatinine 24 h after reperfusion after treatment

7 ed with a ninefold increase in the levels of plasma creatinine 24 h after reperfusion as compared wit

8 chemia significantly decreased the levels of plasma creatinine 24 h after reperfusion as compared wit

9 ere collected once a week after grafting for plasma creatinine, allo-specific antibodies, and protein

10 ed a significant increase in albuminuria and plasma creatinine and a concurrent decrease in circulati

11 miology Collaboration equation based on both plasma creatinine and cystatin C.

12 cisions of the thymus induced an increase in plasma creatinine and histological rejection in 1 of 3 a

13 es between groups were apparent in both mean plasma creatinine and mean creatinine clearance; mean (S

14 5 +/- 147 pg/ml; plasma potassium was lower; plasma creatinine and proteinuria (78 +/- 7 mg/d) were g

15 um fused to the remnant kidney and had lower plasma creatinine and urea nitrogen levels; less glomeru

16 c nephropathy (mesangial expansion, elevated plasma creatinine and urea, decreased creatinine clearan

17 ral morphometry and the utility of measuring plasma creatinine and urinary albumin, has been almost e

18 ne systolic blood pressure, urinary albumin, plasma creatinine, and Indian-Asian ethnicity.

19 bleeding were age >75 years, anemia, raised plasma creatinine, and planned long-term anticoagulation

20 Using plasma creatinine as outcome could reduce the sample siz

21 al impairment as reflected by an increase in plasma creatinine, associated with acute tubular damage

22 ated with the glomerular filtration rate and plasma creatinine but not with mean arterial pressure.

23 ance rate was 22.7 (5.2) mL/min and the mean plasma creatinine clearance rate was 20.7 (4.8) mL/min.

24 Estimated GFR and 24-hr plasma creatinine clearance underestimate GFR with great

25 content as well as a significant increase in plasma creatinine concentration and a reduced capacity o

26 with the risk of renal outcomes (doubling of plasma creatinine concentration and/or progression to en

27 Dogs were killed when the plasma creatinine concentration exceeded 7 mg/dL.

28 en of 13 grafts were surviving with a median plasma creatinine concentration of 185 mumol/L (range 10

29 -proven idiopathic membranous nephropathy, a plasma creatinine concentration of less than 300 mumol/L

30 gorized on the basis of their peak (maximum) plasma creatinine concentration recorded in the first 24

31 loss and kidney function reduction (rise in plasma creatinine concentration); albuminuria was also g

32 alphaT completely prevented the increase in plasma creatinine concentration, the decrease in urinary

33 is or peritoneal dialysis), and missing peak plasma creatinine concentration.

34 rgement, medullary congestion, and a reduced plasma creatinine concentration.

35 critically ill patients, low admission peak plasma creatinine concentrations are independently assoc

36 splantation (n=20) had significantly greater plasma creatinine concentrations at posttransplant days

37 Regression analysis identified that peak plasma creatinine concentrations less than 60 mumol/L me

38 Elevated plasma creatinine concentrations were associated with ma

39 greater mortality and prolonged elevation of plasma creatinine correlating with less tubular epitheli

40 l; change in kidney weight; 0, 24, and 72 hr plasma creatinine (CR); urea nitrogen (BUN); thromboxane

41 as assessed 24 h later (blood urea nitrogen, plasma creatinine [Cr], and renal histology).

42 s later, there was no subsequent increase in plasma creatinine, decrease in glomerular filtration rat

43 evelop kidney damage, evidenced by increased plasma creatinine, decreased kidney weight/body weight r

44 Plasma creatinine did not change with diabetes or SU5416

45 tients surviving one year after trial entry, plasma creatinine exceeded the baseline by more than 25%

46 rated by its analysis of GFRs underlying the plasma creatinine fluctuations in several scenarios of A

47 a dose-dependent decrease in proteinuria and plasma creatinine for the entire 90-day period after tra

48 A2A-KO-->WT chimera, but reduced the rise in plasma creatinine from IRI by 75% in WT mice and by 60%

49 rsening renal function, defined as a rise in plasma creatinine >/=26.5 mumol/l or 50% higher than the

50 Plasma creatinine had strong longitudinal correlations w

51 Control animals had a stable plasma creatinine, had donor-specific unresponsiveness i

52 renal function showed a significantly higher plasma creatinine in HO-1(-/-) mice compared with HO-1(+

53 mocysteine are significantly correlated with plasma creatinine in patients.

54 ure-induced sepsis was effective in reducing plasma creatinine in this model of AKI.

55 Plasma creatinine, inflammation markers (e.g., TNF-alpha

56 Plasma creatinine is a predictor of survival in amyotrop

57 Plasma creatinine is an inexpensive and easily accessibl

58 creatinine is stable, but do not work if the plasma creatinine is changing rapidly.

59 equations estimate kidney function when the plasma creatinine is stable, but do not work if the plas

60 ity to estimate the kidney function when the plasma creatinine is varying acutely.

61 defined as stage 2 or 3 acute kidney injury (plasma creatinine level >/=2 times the baseline level or

62 ment of acute kidney injury according to the plasma creatinine level alone failed to identify acute k

63 al 20-HETE levels after ischemia and reduced plasma creatinine levels (+/-SEM) 24 hours after IR from

64 Increased MDA and plasma creatinine levels also became evident after 4 hou

65 Renal graft function was assessed by plasma creatinine levels and histologic analyses.

66 Plasma creatinine levels and renal inflammation, necrosi

67 alt protoporphyrin prevented the increase in plasma creatinine levels and tubulointerstitial and micr

68 fter slow BD induction, superoxide, MDA, and plasma creatinine levels increased further, whereas GPx

69 Plasma creatinine levels rose transiently with complete

70 d heme-oxygenase 1 expression, and increased plasma creatinine levels were evident.

71 g/hr [95% CI, 0.4-1.2], p = 0.001) and lower plasma creatinine levels.

72 xygenase 1 expression, and increased MDA and plasma creatinine levels.

73 h after reperfusion as compared with normal plasma creatinine levels; however, administration of CO

74 Plasma creatinine may, therefore, increase the power to

75 ance technique and adds the convenience of a plasma creatinine measurement.

76 thout albuminuria (n = 4,031) or with normal plasma creatinine (n = 5,032) at diagnosis.

77 t of WRF, defined as a sustained increase in plasma creatinine of 0.5 mg/dl or >/=50% above first val

78 for 92 (87) months (mean [median]) and has a plasma creatinine of 178 (161) micromol/L, whereas the n

79 o effect on hematologic changes, the rise in plasma creatinine, or lung myeloperoxidase content.

80 quantitative difference between consecutive plasma creatinines over a given time.

81 However, in these patients plasma creatinine (Pcr) is inaccurate and the place of s

82 IRI produced a rise in plasma creatinine (PCr) levels in mice receiving no cell

83 Renal function as determined by plasma creatinine, proteinuria, and glomerular structura

84 lectomy did not show changes in body weight, plasma creatinine, sodium and potassium, and daily urina

85 een patients in rate of decline was lower in plasma creatinine than in ALS functional rating scale-Re

86 ormula variables needed are any steady-state plasma creatinine, the corresponding eGFR by an empirica

87 rawal patients showed a further rise in mean plasma creatinine to 160 (44) and 161 (65) mumol/L at tw

88 AKI attenuated renal injury, as assessed by plasma creatinine, tubular necrosis, and apoptosis.

89 fusion significantly attenuated increases in plasma creatinine, tubular necrosis, macrophage infiltra

90 After 24 hours of reperfusion, we measured plasma creatinine, urea, and histological kidney injury.

91 ifested by increases in blood urea nitrogen, plasma creatinine, urinary N-acetyl-beta-(d)-glucosamini

92 ine and mean creatinine clearance; mean (SD) plasma creatinine values at entry, immediately after wit

93 Plasma creatinine values were lower in the hyperoxia gro

94 e clearance as estimated from mass, age, and plasma creatinine was a significant predictor of BFI on

95 Plasma creatinine was higher in diabetic CTGF+/+ group (

96 Twenty-four h later, plasma creatinine was measured.

97 Plasma creatinine was significantly greater in A2A-KO th

98 l decline, muscle strength and survival with plasma creatinine were assessed.

99 e rejection episodes, insidious increases in plasma creatinine were observed more frequently in this

100 fraction of total glomerular tuft area, and plasma creatinine were significantly higher in D-WT but